RETRACTED: Protein kinase C is a calcium sensor for presynaptic short-term plasticity

• Published in: eLife 2014-08, Vol.3
• Main Authors: Fioravante, Diasynou, Chu, YunXiang, de Jong, Arthur PH, Leitges, Michael, Kaeser, Pascal S, Regehr, Wade G
• Format: Article
• Language: English
• Subjects: Animal genetic engineering; calcium; Enzymes; Genetically modified organisms; Mice; phorbol ester; post-tetanic potentiation; protein kinase C; Protein kinases; short-term plasticity; synaptotagmin
• ISSN: 2050-084X; 2050-084X
• DOI: 10.7554/eLife.03011

In presynaptic boutons, calcium (Ca.sup.2+) triggers both neurotransmitter release and short-term synaptic plasticity. Whereas synaptotagmins are known to mediate vesicle fusion through binding of high local Ca.sup.2+ to their C2 domains, the proteins that sense smaller global Ca.sup.2+ increases to produce short-term plasticity have remained elusive. Here, we identify a Ca.sup.2+ sensor for post-tetanic potentiation (PTP), a form of plasticity thought to underlie short-term memory. We find that at the functionally mature calyx of Held synapse the Ca.sup.2+-dependent protein kinase C isoforms [alpha] and [beta] are necessary for PTP, and the expression of PKC[beta] in PKC[alpha][beta] double knockout mice rescues PTP. Disruption of Ca.sup.2+ binding to the PKC[beta] C2 domain specifically prevents PTP without impairing other PKC[beta]-dependent forms of synaptic enhancement. We conclude that different C2-domain-containing presynaptic proteins are engaged by different Ca.sup.2+ signals, and that Ca.sup.2+ increases evoked by tetanic stimulation are sensed by PKC[beta] to produce PTP.